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First published online August 9, 2006
doi: 10.1242/10.1242/jcs.03156

Journal of Cell Science 119, 3265-3272 (2006)
Published by The Company of Biologists 2006
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Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors

Antonio E. Rusiñol and Michael S. Sinensky*

Department of Biochemistry and Molecular Biology, Box 70581, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37164-0581, USA


Figure 1
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  		Fig. 1. Maturation pathway of prelamin A. Steps A-C are common to all CAAX proteins. Notice that there are two endoproteolytic cleavages for prelamin A - Step A and Step D.

 

Figure 2
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  		Fig. 2. (A,B) Expected C-terminal fragments of (A) wild-type prelamin A and (B) progerin after trypsin digestion. Relative molecular masses were calculated using average masses of the occurring residues and giving masses as [M+H]+.

 

Figure 3
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  		Fig. 3. (A-C) Subnuclear distribution of wild-type and mutant prelamin A. (A) Wild-type EGFP-prelamin A, (B) prenylation-incompetent mutant prelamin A (661C->M) and, (C) step-D-incompetent prelamin-A-EGFP-progerin were transiently expressed in HeLa cells and imaged live (A,C) or after indirect immunofluorescence with anti-prelamin A antibodies (B). Digital images taken by light-microscopy and digital deconvolution are shown.

 




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